The α2/δ Subunit of Calcium Channels – A Multitasking Protein


Kelly Garcia, Liliana Grajales, Tammy Tamayo and Jesús García
University of Illinois at Chicago, Chicago, IL, USA

Series: Protein Biochemistry, Synthesis, Structure and Cellular Functions
BISAC: MED060000

The α2/β subunits form part of voltage-dependent calcium channels and as such are considered accessory proteins. Initial inquiries into the function of α2/β subunits revealed that they modify the voltage dependence, amplitude and kinetics of calcium currents. α2/β subunits have also been identified as the receptor for gabapentin and pregabalin, drugs clinically used in the treatment of several neuropathic disorders. In addition to mediating therapeutical mechanisms, the involvement of α2/β subunits in diseases has been demonstrated in mouse models with mutations of the protein or alterations in expression levels. This book reviews the influence of α2/β subunit in setting the biophysical properties of calcium channels, the connection of α2/β with diseases, and the functions of α2/β that are now being unraveled. (Imprint: Nova)


Table of Contents

Table of Contents


The α2/β; subunits are encoded by four genes

The α2/β subunit is part of voltage-dependent calcium channels

The arrangement of the α2/β subunit in the membrane gives clues as to its interaction with α2/β

The effects of the α2/β subunit on calcium currents depend on the experimental conditions

Role of the α2/β subunit on calcium release

The structure of the α2/β subunit provides evidence for a yet unidentified role of the α2/β; subunit in extracellular signaling

Developmental differences in expression and localization of α2/β -1 and α2/β subunits indicate that these proteins do not always interact with each other

The α2/β subunits interact with other cellular components in addition toα2/β subunits

Link between α2/β subunits and disease




Publish with Nova Science Publishers

We publish over 800 titles annually by leading researchers from around the world. Submit a Book Proposal Now!